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Hypercalciuria from acid load: renal mechanisms.

O W Moe¹, C-L Huang

¹Charles and Jane Pak Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, TX, USA. Orson.Moe@UTSouthwestern.edu

Journal of Nephrology

|June 1, 2006

Summary

Excessive acid load increases kidney stone and osteoporosis risk by causing calcium loss in the kidneys. This review details how acid impacts calcium handling in different kidney tubule segments.

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Area of Science:

Nephrology
Metabolic Bone Disease
Renal Physiology

Background:

Excessive dietary acid load is a recognized risk factor for nephrolithiasis (kidney stones) and osteoporosis.
The complex mechanisms linking acid load to these conditions are not fully understood.
A key proposed mechanism involves increased renal calcium excretion (calcium leak).

Purpose of the Study:

To summarize the current understanding of how acid load affects renal calcium handling.
To explore the specific roles of the proximal tubule, thick ascending limb, and distal convoluted tubule in acid-induced calcium loss.

Main Methods:

Literature review and synthesis of existing research on acid-base balance and renal calcium transport.
Analysis of physiological mechanisms governing calcium reabsorption in different nephron segments.
Integration of data on the impact of acid load on cellular calcium transport processes.

Main Results:

Acid load promotes urinary calcium excretion by impairing reabsorption in the proximal tubule and thick ascending limb.
Reduced hydrogen ion (H+) excretion capacity can exacerbate calcium loss.
Specific transporters and channels involved in renal calcium handling are affected by acid-base status.

Conclusions:

Acid load significantly disrupts normal renal calcium handling, contributing to kidney stone formation and bone demineralization.
Understanding these mechanisms is crucial for developing therapeutic strategies.
Targeting renal calcium handling pathways may offer new avenues for managing nephrolithiasis and osteoporosis.